Akoulitchev S, Mäkelä T P, Weinberg R A, Reinberg D
Howard Hughes Medical Institute, Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854-5635, USA.
Nature. 1995 Oct 12;377(6549):557-60. doi: 10.1038/377557a0.
An array of tandem heptapeptide repeats at the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II constitute a highly conserved structure essential for viability. Studies have established that the CTD is phosphorylated at different stages of the transcription cycle, and that it may be involved in transcriptional regulation. The exact role of the CTD remains elusive, as in vitro reconstituted transcription using the adenovirus major late promoter does not require the CTD. Previous studies showed that transcription from the murine dihydrofolate reductase (DHFR) promoter can be only accomplished by the form of RNA polymerase II that contains the hypophosphorylated CTD (RNAPIIA), but not by the form that lacks it (RNAPIIB). Here we show that the CTD, but not its phosphorylation, is required for initiation of transcription. We also show that transcription requires CTD kinase activity provided by the CDK subunit of TFIIH.
RNA聚合酶II最大亚基的羧基末端结构域（CTD）上的一系列串联七肽重复序列构成了一个对细胞存活至关重要的高度保守结构。研究表明，CTD在转录周期的不同阶段会发生磷酸化，并且可能参与转录调控。CTD的确切作用仍然难以捉摸，因为使用腺病毒主要晚期启动子进行的体外重组转录不需要CTD。先前的研究表明，从小鼠二氢叶酸还原酶（DHFR）启动子进行的转录只能由含有低磷酸化CTD的RNA聚合酶II形式（RNAPIIA）完成，而不能由缺乏它的形式（RNAPIIB）完成。在这里，我们表明转录起始需要CTD，而不是其磷酸化。我们还表明转录需要TFIIH的CDK亚基提供的CTD激酶活性。
